S100A8 and gastric cancer: A mechanism for the development of gastric cancer is that severe oxidative stress in the gastric mucosa in response to H. pylori colonization leads to increased protein expression of virulence factors (CagA, VacA, and AlpA) that cause repeated inflammation of gastric epithelial cells and increased production of antioxidant enzymes (AhpC, KatA, and HtrA) to protect H. pylori [85].